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Chloride and Its Clinical Implications in Today's Clinical Practice: Not an Orphan Electrolyte

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Chloride and Its Clinical Implications in Today's Clinical Practice: Not an Orphan Electrolyte rology & h T ep h e Goel, J Nephrol Ther 2015, 5:6 N r f a o p l e a u DOI: 10.4172/2161-0959.1000223 n t r i c u s o J ISSN: 2161-0959 Journal of Nephrology & Therapeutics Review Article Open Access Chloride and its Clinical Implications in Today’s Clinical Practice: Not an Orphan Electrolyte Narender Goel* Middletown Medical PC, 111, Maltese Drive, Middletown NY, USA; Consultant at Orange Regional Medical Center, NY, USA; Adjunct Clinical Assistant Professor (Internal Medicine and Nephrology) at Touro College of Osteopathic Medicine, New York, USA Abstract Though chloride is the predominant extracellular anion, it is mostly seen just as an anion accompanying sodium and hardly receives attention in textbooks. But independent evaluation of serum chloride may unearth several clinical and acid-base disorders. It is used in formulas to estimate serum anion gap, urine anion gap, and strong ion difference (Stewart method). Several critical functions of a cell such as maintenance of cell volume, neutralization of H+ in lysosomal vesicles, epithelial fluid transport, change in cell membrane potential and ligand-gated transmission in the post-synaptic membrane utilize chloride channels. In addition, chloride forms an integral part of anion exchanger proteins coded by SLC26A gene family. Chloride is an essential component of intravenous fluids used in day-to-day clinical practice. The role and contribution of chloride rich fluids and resulting acidosis in causing inferior outcomes in sepsis, renal vasoconstriction, and acute kidney injury has been debated. Numerous genetic diseases are known to be related with chloride channels and proteins abnormalities. In the following review, I would like to bring much needed attention towards importance of chloride in human physiology. The following hypothetical clinical case will be just a spark for fiery chloride. Keywords: Hyperchloremia; Hypochloremia; Anion exchanger; receives attention in textbooks. But, independent evaluation of serum Chloride channel chloride may unearth several clinical and acid-base disorders. Chloride significantly contributes to plasma tonicity and is used in formulas to Introduction estimate serum anion gap, urine anion gap, and strong ion difference (Stewart method) [3] which is less popular for use in clinical practice Case 1: An 18 years old male was brought to ER in an obtunded state. due to its complex interpretations. He had an alcoholic smell on his breath and was hemodynamically stable with a blood pressure (BP) of 110/60 mmHg. His physical examination Urine Anion Gap = urine [Na+ + K+] – Cl– ------------------ (eq.4) was unremarkable except for him being drowsy. Preliminary laboratory Strong ion difference = (Na+ + K+ + Mg++ + Ca++) – (Cl– + lactate + results were as follows; Serum sodium 139 meq/L, potassium 5 meq/L, other strong anions) ------------------ (eq.5) bicarbonate 22 meq/L, chloride 87 meq/L and glucose of 90 mg/ dL. Blood alcohol level was undetectable and urine microscopy was Na+, K+, Cl–, HCO3– in meq/L significant for oxalate crystals. A diagnosis of poisoning with anti- The role of chloride in urine anion gap measurements is unique freeze (ethylene glycol) was made. + and indirect as chloride here is serving as a surrogate marker of NH4 In this patient most of these laboratory information seems excretion in urine. A positive urine anion gap in the presence of normal however serious acid-base disorder can be easily overlooked metabolic acidosis is often abnormal and points towards low urinary + if attention is not paid towards the remarkably low chloride value NH4 excretion, thus impaired urinary acid excretion. which is suggesting here a complex acid base disorder with high anion gap metabolic acidosis (serum anion gap of 30) and superimposed Chloride Physiology metabolic alkalosis (delta gap of 18 and delta ratio of 10). The high During early experiments, hyperchloremia was found to be anion gap pointed towards unmeasured anions which were later found associated with renal vasoconstriction and fall in glomerular filtration to be oxalic acid, the metabolite of ethylene glycol. rate that was independent of renal sympathetic nervous activity [4]. Serum Anion Gap = serum Na+ – [Cl– + HCO3–] ---------------- Now it is known that functions and physiochemical actions of chloride -- (eq.1) are mediated via chloride channels (ClC), which participates in several critical functions of a cell such as maintenance of cell volume (volume Delta gap= Measured anion gap – Normal anion gap – sensitive ClC), neutralization of H+ in lysosomal vesicles (ClC3, ClC5, Normal [HCO3–] – Measured [HCO3–] ------------------ (eq.2) ClC7), epithelial fluid transport (CFTR, ClC-Ka, ClC-Kb), change in cell membrane potential (ClC1, ClC2, calcium-ClC) and ligand gated ------- (eq.3) *Corresponding author: Narender Goel, Middletown Medical PC, 111, Maltese Na+, Cl– and HCO3– in meq/L Drive, Middletown NY-10940, USA, Tel: +1 845-342-4774; Fax: +1 845-343-8116; E-mail: [email protected] Chloride is the predominant extracellular anion with normal Received: October 01, 2015; Accepted: October 29, 2015; Published: November 05, 2015 concentration ranging from 94-111 meq/L [1]. It is commonly ingested as table salt (sodium chloride). In early experiments, it was determined Citation: Goel N (2015) Chloride and its Clinical Implications in Today’s Clinical Practice: Not an Orphan Electrolyte. J Nephrol Ther 5: 223. doi:10.4172/2161- that chloride’s total body concentration was 30 meq/Kg body weight 0959.1000223 and intracellular concentration was 24.8 meq/L of cell water which Copyright: © 2015 Goel N. This is an open-access article distributed under the was 29.7% (range 19.8-40.4%) of total body chloride [2]. Chloride terms of the Creative Commons Attribution License, which permits unrestricted is mostly seen just as an anion accompanying sodium and hardly use, distribution, and reproduction in any medium, provided the original author and source are credited. J Nephrol Ther Volume 5 • Issue 6 • 1000223 ISSN: 2231-0959 JNT, an open access journal Citation: Goel N (2015) Chloride and its Clinical Implications in Today’s Clinical Practice: Not an Orphan Electrolyte. J Nephrol Ther 5: 223. doi:10.4172/2161-0959.1000223 Page 2 of 4 transmission in the post-synaptic membrane (GABA and glycine anion exchanger-1) plays crucial role in red blood cells in maintaining channels) [5-7]. In the mouse models, function of aquaporin-6 is also electro-neutrality [11]. Another unique chloride channel is cystic shown to involve chloride transport [7]. Macula densa cells perform fibrosis transmembrane conductance regulator (CFTR) that is a located their crucial function of tubuloglomerular feedback by sensing chloride in apical membrane of epithelia and involved in transepithelial salt concentration in tubular fluid [8]. Chloride also forms an integral transport, fluid flow, and ion concentration [12]. Parchorin is a recently part of SLC26A anion exchanger protein. Chloride is also an essential discovered intracellular chloride channel in water secreting cells such component of intravenous fluids used in day-to-day clinical practice as salivary glands, lachrymal glands, pancreas, cochlea and kidneys and it concentration in different replacement fluids (mmol/L) is as whereby it plays a critical role in water secretion by regulation of follows [1]: chloride transport. Prestin is another SLC25A5 gene encoded chloride/ bicarbonate anion exchanger protein and present on outer hair cells of 4% Albumin= 128; Normal saline (0.9%) = 154, Half normal saline cochlea [13]. (0.45%) = 77, Ringers lactate= 111, PlasmaLyte= 98, Hydroxyethyl starch= range 110-154 Causes of chloride disorders Finally, the role and contribution of chloride rich fluids and Hypochloremia: Low serum chloride is often associated with resulting acidosis in causing inferior outcomes in sepsis [3], renal metabolic alkalosis that could be due to volume loss from gastric vasoconstriction [3] and acute kidney injury [9] has been debated [3]. content as gastric fluid is rich in chloride (Cl–) along with proton (H+) both of which together forms hydrochloric acid [3] or from kidneys Handling of chloride by the kidneys such as due to diuretics or salt wasting nephropathies (Bartter and Approximately 21000 meq of chloride is filtered everyday of which Gitelman Syndrome) [14]. >99% is absorbed (55% in proximal tubule, 25-35% in thick ascending In these cases, chloride depletion also plays a crucial role in loop (TAL) of Henle and rest in distal tubule) and only 100-250 meq is maintaining metabolic alkalosis. Decreased delivery of chloride to the excreted every day [10]. Once in proximal tubular lumen, chloride is macula densa stimulates renin release which activates angiotensin and reabsorbed actively via anion exchanger [SLC26A6] (chloride-formate, aldosterone and thereby promotes proton excretion in the distal tubule. chloride-hydroxyl, chloride-oxalate exchanger) on luminal side and + - The lower chloride concentration in the tubular lumen also impairs leave the cells via K Cl co-transporter and chloride selective channels – – activity of luminal Cl -HCO3 exchanger in type B intercalated cell and [10]. Chloride is also reabsorbed passively across tight junctions in – + – leads to reduced excretion of HCO3 , exacerbating metabolic alkalosis proximal tubule [10]. In the proximal tubule, ClC5 (H /Cl antiporter) further. helps to secretes H+ into endosomes and maintain low pH that is necessary for protein degradation [5-7]. Hypochloremia and
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